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RsbV of Listeria monocytogenes contributes to regulation of environmental stress and virulence

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Abstract

SigmaB factor is an important regulatory factor for stress response in Gram-positive bacteria such as Listeria monocytogenes (L. monocytogenes), Staphylococcus aureus and Bacillus subtilis. However, the activity of SigmaB factor is regulated by RsbV factor. Currently, the functional studies of RsbV factor are mostly focused on non-pathogenic B. subtilis, but the roles of RsbV factor in pathogenic L. monocytogenes during the regulation of environmental stress and virulence are still unclear. In the study, a ∆RsbV mutant of L. monocytogenes was constructed to explore the regulatory role of RsbV in environmental stress and virulence. The environmental stress experiments indicated that the growth and survival capability of ∆RsbV mutant obviously decreased in stress of low temperature, osmotic pressure, alcohol and acid, compared with EGD strain. The macrophage infection experiment indicated that ∆RsbV mutant had weaker survival capability than EGD strain, and the expression of PrfA, actA, PlcA and LLO was down-regulated in infected cells. Animal inoculation experiments indicated that RsbV deletion significantly reduced the pathogenicity of L. monocytogenes. Our data demonstrate that, in addition to regulating tolerance under environmental stress conditions, RsbV also contributes to regulation of L. monocytogenes virulence.

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Acknowledgments

We thank the staff from State Key Laboratory of Veterinary Etiological Biology for technical support and the field staff who provided the tick samples for this study. This study was supported by the State Basic Research Development Program of China (973 Program) (No. 2010CB530204; 2010CB530206) and the National Natural Science Foundation of China (No. 30960274; 31260601).

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Correspondence to Qingling Meng or Jun Qiao.

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Communicated by Erko Stackebrandt.

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Zhang, Z., Meng, Q., Qiao, J. et al. RsbV of Listeria monocytogenes contributes to regulation of environmental stress and virulence. Arch Microbiol 195, 113–120 (2013). https://doi.org/10.1007/s00203-012-0855-5

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  • DOI: https://doi.org/10.1007/s00203-012-0855-5

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